Evidence map›Paper›PMID 26269584›Full record

ArticleMolecular biology of the cell2015

Hcm1 integrates signals from Cdk1 and calcineurin to control cell proliferation.

Heather E Arsenault, Jagoree Roy, Claudine E Mapa, Martha S Cyert, Jennifer A Benanti

Erratum issuedAbstract read
In one paragraph

Article in Molecular biology of the cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.6field-weighted citation impact, top 30% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Article
  3. Dynamic phosphorylation of Hcm1 promotes fitness in chronic stress.bioRxiv : the preprint server for biology · 2025
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Mitochondrial Localization of the Yeast Forkhead Factor Hcm1.International journal of molecular sciences · 2020
    Article
  10. Article
  11. Identifying New Substrates and Functions for an Old Enzyme: Calcineurin.Cold Spring Harbor perspectives in biology · 2020
    Review
  12. Review
  13. Calcineurin, the CaMolecular biology of the cell · 2017
    Article
  14. Article
  15. Review
  16. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Heather E ArsenaultDepartment of Molecular, Cell and Cancer Biology, University of Massachusetts Medical School, Worcester, MA 01520.
Jagoree RoyDepartment of Biology, Stanford University, Stanford, CA 94305.
Claudine E MapaDepartment of Molecular, Cell and Cancer Biology, University of Massachusetts Medical School, Worcester, MA 01520.
Martha S CyertDepartment of Biology, Stanford University, Stanford, CA 94305.
Jennifer A BenantiDepartment of Molecular, Cell and Cancer Biology, University of Massachusetts Medical School, Worcester, MA 01520 jennifer.benanti@umassmed.edu.
University of Massachusetts Chan Medical School · USStanford University · US

Funding

YEAST PP2B PHOSPHATASES--ROLE IN PHEROMONE ADAPTATIONR01GM048729 · NIGMS · STANFORD UNIVERSITY · PI CYERT, MARTHA S. · 1993 to 2013
$5.4M
NIGMS NIH HHS R01 GM048729NIGMS NIH HHS R01GM048729
6 · The paper itself

Abstract

Cyclin-dependent kinase (Cdk1) orchestrates progression through the cell cycle by coordinating the activities of cell-cycle regulators. Although phosphatases that oppose Cdk1 are likely to be necessary to establish dynamic phosphorylation, specific phosphatases that target most Cdk1 substrates have not been identified. In budding yeast, the transcription factor Hcm1 activates expression of genes that regulate chromosome segregation and is critical for maintaining genome stability. Previously we found that Hcm1 activity and degradation are stimulated by Cdk1 phosphorylation of distinct clusters of sites. Here we show that, upon exposure to environmental stress, the phosphatase calcineurin inhibits Hcm1 by specifically removing activating phosphorylations and that this regulation is important for cells to delay proliferation when they encounter stress. Our work identifies a mechanism by which proliferative signals from Cdk1 are removed in response to stress and suggests that Hcm1 functions as a rheostat that integrates stimulatory and inhibitory signals to control cell proliferation.

Indexed as

CalcineurinCDC2 Protein KinaseCell ProliferationForkhead Transcription FactorsPhosphoric Monoester HydrolasesPhosphorylationSaccharomyces cerevisiae ProteinsSaccharomycetalesStress, PhysiologicalTranscription FactorsCalcineurinCDC2 Protein KinaseForkhead Transcription FactorsHCM1 protein, S cerevisiaePhosphoric Monoester HydrolasesSaccharomyces cerevisiae ProteinsTranscription Factors

Identifiers

PMID26269584
PMCPMC4603928
OpenAlexW2244996777

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.